A reproducible experimental model of cervical spondylosis in rodents was established by means of detachment of the back paravertebral muscles from the vertebrae and resection of the spinous processes together with supraspinous and interspinous ligaments. Spinal instability elicited by this surgical intervention accelerated the process of intervertebral disc degeneration. It induced cervical spondylosis in mice when extended over a 6 — 12 month period. The pathologic changes in the cervical intervertebral discs of this animal model were progressive: proliferation of cartilaginous tissue and fissures in the annulus fibrosus; shrinkage or disappearance of the nucleus pulposus; and herniation of disc materials and osteophyte formation.
Basic fibroblast growth factor (bFGF) was reported to stimulate proliferation and matrix synthesis of cultured intervertebral disc cells. Using this animal model, the distributions of cells expressing bFGF and FGF receptor (FGF-R) were investigated in normal and degenerating intervertebral discs by immunohistochemistry and in situ hybridization histochemistry. Expression of bFGF protein and FGF-R messenger RNA were found in actively proliferating chondrocytes in the degenerating annulus fibrosus, whereas these were negative in normal annulus fibrosus. This suggested that bFGF might regulate the process of disc degeneration.
The availability of this experimental model should be valuable for further understanding, both biochemically and biomechanically, of the pathogenesis of cervical spondylosis.